Abstract
To gain more insight into the human metabolism of the essential trace element selenium, we investigate the response of the urinary selenium metabolites to changing selenium intake by applying a stepwise selenium administration regimen based on repeated dosaging. Sodium selenite was administered orally to healthy volunteers at an incrementally increasing dosage. The supplementation regimen extended over 20 days for each volunteer, and daily morning urine samples were collected prior to, during, and following the supplementation phases. A total of 160 urine samples were analyzed for total urinary selenium and a panel of selenometabolites by using ICPMS and HPLC/ICPMS. Selenosugar 1 gave the strongest response followed by TMSe and then selenosugar 3. Se-methylselenoneine excretion was not stimulated by increased selenium intake, suggesting that it is not in equilibrium with selenium body pools. Selenate was detected in all urine samples; it showed a clear and consistent response to supplementation and an abrupt return to baseline levels upon cessation of supplementation, indicating that it arose from the oxidation of the administered selenite rather than from the oxidation of endogenous hydrogen selenide. The gap between total urinary selenium and the sum of Se species markedly increased in response to selenium administration, which highlights the presence of unknown Se species that respond to selenite supplementation. The characterization of these unknown species and their possible biological activities might be essential before considering selenium supplementation in clinical trials. We discuss the implications of the responses of the selenium metabolites and their inter-relationships for selenium metabolism.
Highlights
Despite selenium’s low abundance in the earth’s crust, the catalytic advantages of replacing sulfur by selenium in selenoproteins warranted the evolution of a highly complicated mechanism for the co-translational insertion of selenocysteine, the 21st amino acid, in proteins in response to a stop codon.[1]On the other hand, the high specificity of these advantages is reflected by the limited number of known selenoproteins.[2] the essentiality of selenium was first recognized over 60 years ago,[3] only little is known about the biotransformation pathways and enzymatic systems involved in the metabolism of selenium (Fig. 1)
The essentiality of selenium was first recognized over 60 years ago,[3] only little is known about the biotransformation pathways and enzymatic systems involved in the metabolism of selenium (Fig. 1)
Very little is known about other possible fates of the central selenium species hydrogen selenide, and a large gap between the sum of identified urinary selenium species and total urinary selenium has been consistently reported.[12,13]
Summary
Exploring the urinary selenometabolome following a multi-phase selenite administration regimen in humans†. The supplementation regimen extended over 20 days for each volunteer, and daily morning urine samples were collected prior to, during, and following the supplementation phases. The gap between total urinary selenium and the sum of Se species markedly increased in response to selenium administration, which highlights the presence of unknown Se species that respond to selenite supplementation. The characterization of these unknown species and their possible biological activities might be essential before considering selenium supplementation in clinical trials. We discuss the implications of the responses of the selenium metabolites and their inter-relationships for selenium metabolism
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